Just before the sun began its slow descent below the horizon on April 22, 1915, thousands of German soldiers simultaneously twisted the knobs on metal cylinders containing chlorine gas. They released a rolling cloud that tumbled across “no man’s land” and into the unprepared trenches of the British Expeditionary Force defending the line at Ypres, France. Thousands died. In this first use of modern chemical warfare, all the advantages lay with the attacker. The British had no gas masks, their physicians did not know how to treat gas-related casualties, and their hospital infrastructure was not equipped to handle the strain of thousands of new patients. While the German military offensive floundered, medically Ypres was a disaster for the British and French. Over the next three years, warring countries worked to develop multi-tiered responses to the threat of chemical weapons.
U.S. advances technology and treatment
Since the U.S. did not enter World War I until 1917, it benefitted from the lessons learned by the French and British. The U.S. Army Medical Department (AMEDD) created a Chemical Warfare Service (CWS) to develop protective equipment, which allowed its physicians to focus on treatment.1,2 The CWS created an array of technologies to protect soldiers. Initially forced to adopt British small-box respirators when early American gas masks proved ineffective, the U.S. invested in a massive research effort, eventually deploying the Kops-Tissot-Monroe mask that became standard issue. The U.S. ultimately produced more than 5 million gas masks.2-4
The Army also devised numerous detectors that variously alarmed, beeped, and changed color in the presence of poison gas.3,4 Although it was recognized that North American snails frantically waved their tentacles when exposed to gas, this technique did not prove to be a practical warning device.5
Once in Europe, AMEDD adopted the French “Z” system of evacuation, assigning one hospital per division to specialize in the care of chemical weapons victims (see Figure 1).1 AMEDD also deployed mobile decontamination units, which could cleanse 24 men every three minutes. When the men stripped to shower, medical officers examined their skin for evidence of gas exposure, triaging individuals who needed further care at specialized facilities (see Figure 2).3,5
Figure 1. AMEDD advance gas aid station
Source: National Museum of Health and Medicine, Otis Historical Archives, OHA 342, Box 7 of U.S. Army Signal Corps Photographs
Figure 2. Plan of Mobile Degassing Station
Source: U.S. Army Medical Department Office of Medical History. Available at: http://history.amedd.army.mil/booksdocs/wwi/VolXIV/Figures/FIG01.pdf.
While extensive research delineated the pathophysiology of chemical weapons, therapeutic options remained few in number and largely ineffective. Physicians prioritized minimizing exposure, keeping casualties warm, providing pain control, and allowing them rest. The literature proposed innumerable salves to ameliorate the skin burns caused by mustard gas, but none proved especially beneficial. Physicians did try using Dakin’s solution to wash off mustard gas residue but found petroleum equally effective and readily available on the battlefield.1
The pulmonary effects of chemical warfare proved the most lethal (see Figure 3). Gases caused severe edema and killed the cells lining the respiratory tract, leaving necrotic tissue to slough off and fill the lungs. In an era before antibiotics, and in a population weakened by the exposure, malnutrition, and influenza so prevalent on 1918 battlefields, patients developed pneumonia and congestive heart failure and died. Resorting to an ancient therapy, physicians bled patients, believing the phlebotomy would reduce the strain on the heart and help the body absorb secretions from the lungs.1 Inhalation oxygen therapy was used infrequently, improperly (at least in retrospect), and provided little benefit.
Figure 3. Mustard-gas lesions of tongue, pharynx, larynx, and trachea, in fatal human case
Dorsum of tongue shows diphtheritic eschars. Diphtheritic necrosis of pharynx, mucosa of larynx, and trachea. Marked edema, with diphtheritic necrosis of the arytenoepiglottidean fold.
Source: U.S. Army Medical Department Office of Medical History. Available at: http://history.amedd.army.mil/booksdocs/wwi/VolXIV/Figures/FIG201.pdf.
Interestingly, after the war, a diverse group of military officers, physicians, and veterans organizations such as the American Legion campaigned for increased use of chemical weapons in future conflicts, vociferously arguing that they were more humane and less lethal than traditional armaments.1 Largely for strategic reasons, armies in World War II did not deploy poison gas against each other, although the Axis Powers did use it to murder civilians in concentration camps across Europe and in prisoner-of-war camps in Asia.
- Bancroft WD, Bradley HC, Eyster JAE, et al. Medical Aspects of Gas Warfare. Washington, DC: U.S. Government Printing Office; 1926.
- Brophy LP, Miles WD, Cochrane RC. The Chemical Warfare Service: From Laboratory to Field. Washington, DC: Center of Military History; 1959.
- Joy RJT. Historical aspects of medical defense against chemical warfare. In: Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General; 1997: 87-110.
- Smart JK. History of chemical and biological warfare: An American perspective. In: Medical Aspects of Chemical and Biological Warfare. Washington, DC: Office of the Surgeon General; 1997:9-86.
- Fries AA, West CJ. Chemical Warfare. New York, NY: McGraw-Hill Book Company, Inc.; 1921.